Evidence of endothelial dysfunction in coronary resistance vessels in patients with angina pectoris and normal coronary angiograms

Motz, W.; Vogt, M.; Rabenau, Oliver; Scheler, Sibylle; Lückhoff, Andreas; Strauer, Bodo E.

doi:10.1016/0002-9149(91)90485-4

Cited by 219 publications

(83 citation statements)

References 22 publications

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“…Histopathological examinations of endomyocardial biopsies of patients with CSX have shown structural abnormalities of small coronary vessels including medial hypertrophy and luminal narrowing (15). Both endothelium dependent and independent vasodilatation are altered in patients with CSX (16,17). Vasoconstrictor activity and inflammatory markers are increased in CSX patients (18,19).…”

Section: Introductionmentioning

confidence: 99%

Assessment of cardio-ankle vascular index in patients with cardiac syndrome-X: an observational study

Aykan¹,

Gökdeniz²,

Gül³

et al. 2013

Anadolu Kardiyol Derg

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Objective: Arterial stiffness is associated with major adverse cardiovascular events. Cardio-ankle vascular index (CAVI), a novel marker of arterial stiffness, which is weakly influenced by systolic blood pressure, is a sensitive marker the atherosclerosis and arteriolosclerosis. The aim of this study is to investigate arterial stiffness by CAVI in patients with cardiac syndrome X (CSX). Methods: The present study was observational and cross sectional, and involved 49 patients (26 male) with CSX (angina-like chest pain, positive electrocardiographic ischemic changes at treadmill exercise test, angiographically normal coronary arteries) and 54 healthy subjects (21 male). CAVI was measured by VaSera-1000 CAVI instrument. Statistical analysis was performed using the Chi-square, Student t-test, correlation analysis and logistic regression analysis. Results: The CAVI and pulse pressure were significantly increased in patients with CSX compared to control group (7.50±1.50, 6.49±0.77, p<0.001; 53.00±10.06, 47.39±8.17, p=0.002, consecutively). In contrast, there were no significant differences in the age, weight, height, body mass index, waist circumference, hip circumference, systolic blood pressure, diastolic blood pressure, mean blood pressure, glucose, low density lipoprotein level, high density lipoprotein level (HDL), triglyceride, estimated creatinine clearance, hemoglobin, left atrium diameter, left ventricular mass (LVM), LVM index and ejection fraction. CAVI was the only independent predictor of CSX in logistic regression analysis (OR=1.780, 95% CI: 1.157-2.737, p=0.009). Conclusion: CAVI is increased in syndrome X patients and is an independent predictor of this syndrome. (Anadolu Kardiyol Derg 2013; 13: 766-71) Key words: CAVI, arterial stiffness, cardiac syndrome X, coronary, angiography, regression analysis Original Investigation Özgün Araşt›rma 766ÖZET Amaç: Damar sertliği önemli kardiyovasküler kötü hadiselerle ilişkilidir. Kalp-ayak bileği vasküler indeks ölçümü (KAVI), sistolik kan basıncından çok az etkilenir ve damar sertliği değerlendirilmesinde yeni ve hassas bir yöntem olup ateroskleroz ve arteriolosklerozun hassas bir gösterge-sidir. Bu çalışmanın amacı kardiyak sendrom-X'li hastalarda (KSX) KAVI yöntemi ile damar sertliğinin değerlendirilmesidir. Yöntemler: Çalışmamız gözlemsel ve kesitsel nitelikte olup, bu çalışmada 49 KSX (tipik göğüs ağrısı olan, egzersiz elektrokardiyografi testinde pozitif iskemik değişiklikleri bulunan ve yapılan koroner anjiyografide normal koroner arterler tespit edilen hastalar) (29 erkek) ve 54 sağlıklı hasta (21 erkek) değerlendirildi. KAVI VaSera-1000 KAVI aletiyle ölçüldü. İstatistiksel analizde Ki-kare, t-testi, korelasyon analizi ve mantıksal regresyon analizi kullanıldı. Bulgular: KSX hastalarında KAVI ve nabız basıncı kontrol grubuna göre anlamlı olarak daha yüksekti

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Section: Introductionmentioning

confidence: 99%

Assessment of cardio-ankle vascular index in patients with cardiac syndrome-X: an observational study

Aykan¹,

Gökdeniz²,

Gül³

et al. 2013

Anadolu Kardiyol Derg

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“…At present, the most reasonable mechanism explaining risk associated with LVH is impaired coronary hemodynamics manifested by reduced coronary blood flow and flow reserve associated with increased coronary vascular resistance and minimal coronary resistance (8)(9)(10). Resting coronary hemodynamic parameters need not be impaired, however; but they may become deranged in otherwise asymptomatic individuals by certain physiological or pharmacological interventions (9)(10)(11), reflecting impaired coronary arteriolar dilation engendered by the coronary arteriolar constriction of hypertension, as well as by endothelial dysfunction (12)(13)(14).…”

mentioning

confidence: 99%

“…Frohlich onstrated clinically, as well as experimentally and relates to a defect in the local vascular and myocardial generation of nitric oxide (12)(13)(14). Additional hemodynamic mechanisms which may account for impaired coronary hemodynamics include coronary arteriolar compression by the hypertrophied and stiffer left ventricle (LV) produced by ventricular fibrosis, occlusive atherosclerotic epicardial coronary arterial disease that exacerbates the hypertensive disease, the increased arteriolar wall thickening and arteriolar wall-to-lumen diameter directly characteristic of hypertensive vascular disease (15), inadequate sizing of coronary vessels (16), increased blood viscosity in hypertension (17), and the increased LV chamber diameter reflecting not only myocytic hypertrophy but type 3 collagen deposition (18)(19)(20).…”

mentioning

confidence: 99%

Ischemia and fibrosis: the risk mechanisms of hypertensive heart disease

2000

Braz J Med Biol Res

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Mechanisms underlying risk associated with hypertensive heart disease (HHD) and left ventricular hypertrophy (LVH) are discussed in this report and provide a rationale for understanding this very common and important cause of death from hypertension and its complications. Emphasized are impaired coronary hemodynamics, endothelial dysfunction, and ventricular fibrosis from increased collagen deposition intramurally and perivascularly. Each is exacerbated by aging and, perhaps, also by increased dietary salt intake. These functional and structural changes promote further endothelial dysfunction, altered coronary hemodynamics, and diastolic as well as systolic ventricular contractile function in HHD. The clinical endpoints of HHD include angina pectoris (with or without atherosclerosis of the epicardial coronary arteries), myocardial infarction, cardiac failure, lethal dysrhythmias, and sudden death. The major concept to be derived from these alterations is that not all that is clinically recognized as LVH is true myocytic hypertrophy and structural remodeling. Other major co-morbid changes occur that serve to increase cardiovascular risk including impaired coronary hemodynamics, endothelial dysfunction, and ventricular fibrosis.

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“…The exact etiology, pathogenesis and long term outcome of SCF patients is still unknown. Endothelial and vasomotor dysfunction, microvascular dysfunction, and occlusive disease of small coronary arteries were suggested in its etiology (8)(9)(10)(11)(12)(13)(14)(15)(16)(17). The carotid artery intima-media thickness (CIMT) is the best known sonographic marker for early atherosclerotic vascular wall lesions (18).…”

mentioning

confidence: 99%

Intravascular Ultrasound (IVUS) and Clinical Applications

Özcan¹

2012

Intravascular Ultrasound

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Evidence of endothelial dysfunction in coronary resistance vessels in patients with angina pectoris and normal coronary angiograms

Cited by 219 publications

References 22 publications

Assessment of cardio-ankle vascular index in patients with cardiac syndrome-X: an observational study

Assessment of cardio-ankle vascular index in patients with cardiac syndrome-X: an observational study

Ischemia and fibrosis: the risk mechanisms of hypertensive heart disease

Intravascular Ultrasound (IVUS) and Clinical Applications

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